Smoking is linked to gene expression changes, some of which appear to persist after quitting, researchers found.

Action Points

Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.

Note that this gene expression study reveals different expression profiles among smokers, former smokers, and never smokers.

Be aware that without longitudinal data, the causal link between smoking and gene expression changes can not be confirmed.

Smoking is linked to gene expression changes, some of which appear to persist after quitting, researchers found.

More than 100 genes were expressed significantly differently in smokers than in nonsmokers across two large population-based studies, Roby Joehanes, PhD, of the National Institutes of Health in Bethesda, Md., and colleagues showed.

"These genes were associated with many pathways, including immune response, response to stress, blood coagulation, platelet activation, and apoptosis," the group noted.

Three of these genes showed up as differentially expressed in former smokers as well, they reported at the American Heart Association's Epidemiology and Prevention/Nutrition, Physical Activity and Metabolism meeting in New Orleans.

Some of the pathways were expected, while others appeared novel, the organization's president, Donna Arnett, PhD, MSPH, noted, an epidemiologist specializing in cardiovascular genetics at the University of Alabama at Birmingham.

"We've know for a long time that smoking increases the risk of cardiovascular disease, particularly myocardial infarction. We've also known for long time that it is associated with increased coagulation disorders and platelet aggregation," she told MedPage Today. "The study is showing that also includes genes involved in immune response and in response to stress, which is new. Apoptosis is also a new pathway."

Joehanes's group first compared whole-blood gene expression among 2,446 participants in the Framingham Heart Study after adjusting for sex, age, and family relationships within the cohort.

Self-reported smoking status across 37 years of observation in the study indicated that most used to smoke (1,460) but relatively few still did (204). Another 782 never smoked.

In that cohort, 1,602 genes were expressed significantly different between current and never smokers.

Among those differentially expressed genes, 112 again were associated with smoking in a replication analysis of the San Antonio Family Heart Study.

Replication in a second population adds confidence to the findings, but the single observation is a limitation, Arnett noted.

Without comparing individual before and after smoking initiation, the study couldn't draw causal conclusions.

"There could be other factors associated with smoking that could also explain the results," she pointed out.

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